The chronic oral toxicity of selected isomers of tetrachloro- and hexachlorobiphenyl will be compared in rhesus monkeys. The excreted metabolites of each isomer will be identified, and the kinetics of storage of parent compound in fat and liver and the pattern of hepatic microsomal enzyme induction will be determined for each isomer. The major metabolites of those isomers that are most toxic will be synthesized in quantity and tested for toxic potency in monkeys. The experimental results to date support the hypotheses that (1) only compounds without ortho substitution by chlorine atoms are strongly toxic and cause methylcholanthrene-like enzyme induction, (2) hydroxylation is the dominant mode of metabolism, and (3) persistent storage in fat correlates with the absence of unsubstituted positions in the phenyl rings but not with toxicity.